Are Survivors of Childhood Acute Lymphoblastic Leukemia at Increased Risk for Low Bone Mass?

Abstract

Acute lymphoblastic leukemia is the most prevalent cancer in children. As an increasing number of cancer survivors reaches adulthood, there may be consequences of the treatment, and there is an issue if low bone mass might be included as a significant late effect. Acute lymphoblastic leukemia patients may have their bone mass compromised during therapy and many years after its withdrawal, but the degree of bone mass decline or recovery are not well elucidated to date. Survivors of stem cell transplantation for leukemia have additional risk factors for bone loss and should be evaluated with caution. Our target is to make a warning about the difficulties in assessing and interpreting bone mass in children and adolescents, the limitations in this assessment in acute lymphoblastic leukemia young survivors (including survivors of stem cell transplantation), the possibility of misdiagnoses, the reasons (if there are any) of low bone mass in this particular group of cancer survivors, as well as consider the therapeutic issues available.

Visfatin is a positive predictor of bone mineral density in young survivors of acute lymphocytic leukemia

“…However, only 5.4 % of patients presented with low BMD at the total body site and 8.9 % at the lumbar spine, which is consistent with previous studies showing that the majority of adult longterm ALL survivors had BMD within normal limits [5, 12, [35][36][37]. ALL patients seem to lose bone mass during treatment, increasing their risk of fracture during this period, but usually return to normal range two years after the completion of treatment, and subsequently to the end of the period known as the adiposity rebound [10,36,37]. This fact reinforces the influence of changes in body composition on bone mass [1-6, 24, 25, 28, 29, 31, 32, 37].…”

“…ALL survivors exposed to CRT presented with decreased total body (but not lumbar spine L 1 -L 4 ) BMD and consistently decreased visfatin levels, which in turn positively influenced both trabecular and cortical BMD. It is possible that this relationship may represent an indirect effect of CRT on decreasing BMD through reduced visfatin levels [11,[35][36][37].…”